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Inflammation serves as the body's immune response mechanism against noxious irritants, ranging from removing factors causing injury to regenerating damaged tissue. Chronic inflammation, in particular, has emerged as a crucial contributor to both the development of cancer and its spread through a variety of mechanisms. This phenomenon is referred to as inflammation-induced tumorigenesis. Differing from other forms of inflammation that typically precede tumor formation, 'cancer-elicited inflammation (CEI)' is induced following the initiation of a tumor. Beyond the cell-autonomous effects observed in cancer cells, the activation of several oncogenes, including KRAS and MYC, coupled with the rendering of tumor suppressors, for instance, TP53 inactive, triggers programs at the transcription level that culminate in the formation of a tumor-encouraging microenvironment. This is accomplished by the overproduction of chemokines and pro-inflammatory cytokines, immune cell recruitment, and the initiation of angiogenesis. Although it is critical to comprehend the mechanisms by which inflammation aids in the development of cancer, the impact that tumors themselves have on the immune system must be considered because these effects have significant repercussions for the therapy and prevention of cancer. This comprehensive review primarily centers on various inflammatory pathways that have been influenced by cancer and have, in turn, influenced cancer progression. Additionally, we delve deeply into the intricate mechanisms through which specific natural products exert regulatory control over the complex molecular foundations that drive their robust anti-inflammatory and anti-cancer effects.
Shaw et al. (Wed,) studied this question.